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Transcriptome profiling of lymph nodes from Spink5 conditional knock-out mice.

ABSTRACT: We generated a viable mouse model of Netherton syndrome by conditional ablation of Spink5 gene in the epidermis. To study the systemic inflammation phenotype of this mouse model at the molecular level, we induced Spink5 deletion in the skin of young adult mice and collected inguinal lymph nodes for transcriptome analyses.

ORGANISM(S): Mus musculus

PROVIDER: GSE224409 | GEO | 2024/02/05

REPOSITORIES: GEO

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Transcriptome profiling of lesional skin from Spink5 conditional knock-out mice

Project description:We generated a viable mouse model of Netherton syndrome by conditional ablation of Spink5 gene in the epidermis. To characterize this model at the molecular level, we induced Spink5 deletion in young adult mice and collected lesional skin samples for transcriptome analyses.

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Comparative analyses of Netherton syndrome patients and Spink5 conditional knock-out mice define disease-relevant pathways

Project description:Netherton syndrome (NS) is a rare skin disease caused by loss-of-function mutations in the serine peptidase inhibitor Kazal type 5 (SPINK5) gene. Disease severity and the lack of efficacious treatments call for a better understanding of NS mechanisms. Here we describe a viable, Spink5 conditional knock-out (cKO) mouse model, allowing to study NS progression. Using comparative transcriptomics and proteomics, we determine a disease molecular profile conserved in mouse models and NS patients. Spink5 cKO mice and NS patients share skin barrier and inflammation signatures defined by up-regulation of proteases, IL-17, IL-36, IL-20 family cytokines. Furthermore, we show that systemic inflammation in Spink5 cKO mice is associated with thymic atrophy and is driven by innate immunity and IL-17/IL-22 signaling. By comparing skin transcriptomes and proteomes, we uncovered several putative substrates of tissue kallikrein-related proteases (KLKs), demonstrating that KLKs can proteolytically regulate IL-36 pro-inflammatory cytokines. Our study thus provides a conserved molecular framework for NS disease, adding new insights into its mechanisms and therapeutic targets.

2023-02-02 | MSV000091184 | MassIVE

Transcriptome profiling of lesional skin from neonate Spink5 constitutive knock-out mice

Project description:Spink5 constitituve knock-out mice mimic the disease features of Netherton syndrome but die within several hours after birth due to severe skin barrier defect. To characterize the skin barrier and skin inflammation phenotype of this mouse model at the molecular level, we collected back skin samples from mice shortly after their birth.

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Transcriptome profiling of lymph nodes from Spink5 conditional knock-out mice.

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Transcriptome profiling of lesional skin from Spink5 conditional knock-out mice

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